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Dimethyl Fumarate Protects Diabetes-Induced Testicular Toxicity in Rats: Investigations on Nrf-2/HO-1 and
Asutosh Pattnaik1, Girija Prasanna Sahoo1, Vaishali Maurya1
1Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Facility for Risk Assessment and Intervention Studies, S.A.S Nagar, India.
Abstract:
Type 1 Diabetes Mellitus (T1DM) is associated with the destruction of insulin-producing β-cells and is characterized by prolonged hyperglycemia. This can increase oxidative stress which eventually damages the male reproductive system, disturbs the production of testosterone, alters semen quality and histological architecture, and increases testicular apoptosis. Dimethyl Fumarate (DMF) is an Nrf-2 activator that has been explored as possible protective agent in several preclinical studies, although its exact role in germ-cell toxicity is still not well-known. In the present study, an attempt has been made to elucidate the role of DMF in testicular toxicity in Sprague-Dawley (SD) rats. Animals having fasting blood glucose >250 mg/dl after treatment with Streptozotocin (STZ; 55 mg/kg, i.p) were considered diabetic. Three doses of DMF (12.5, 25, and 50 mg/kg) were administered to the diabetic animals for 4 consecutive weeks. The testicular damage was characterized by evaluating organ index, biochemical and histological parameters, sperm-related indices, DNA strand breaks, and expression of different proteins. The results revealed that treatment with DMF ameliorated diabetes-induced testicular damage by decreasing testicular oxidative stress and apoptosis, increasing testosterone production, and upregulating the expressions of Nrf-2, HO-1, IL-10, β-Catenin, OCT-4, 3β-HSD, Bcl-2 and downregulating NF-κB, Bax. The present finding suggests that DMF has a protective effect against diabetes-induced testicular damage in SD rat.
Insights
Dimethyl Fumarate (DMF) protects against testicular damage caused by Type 1 Diabetes Mellitus (T1DM). This study shows DMF reduces oxidative stress and improves reproductive health in diabetic rats.
Area of Science:
- Endocrinology
- Reproductive Biology
- Toxicology
Background:
- Type 1 Diabetes Mellitus (T1DM) leads to hyperglycemia, oxidative stress, and male reproductive system damage, including altered testosterone production and testicular apoptosis.
- Dimethyl Fumarate (DMF), an Nrf-2 activator, has shown potential protective effects in preclinical studies, but its role in diabetes-induced testicular toxicity is not fully understood.
Purpose of the Study:
- To investigate the protective role of Dimethyl Fumarate (DMF) against testicular toxicity in a rat model of Type 1 Diabetes Mellitus (T1DM).
Main Methods:
- Sprague-Dawley (SD) rats were induced with diabetes using Streptozotocin (STZ).
- Diabetic rats received three doses of DMF (12.5, 25, 50 mg/kg) for four weeks.
- Testicular damage was assessed via organ index, biochemical and histological parameters, sperm quality, DNA damage, and protein expression.
Main Results:
- DMF treatment ameliorated diabetes-induced testicular damage.
- DMF decreased testicular oxidative stress and apoptosis.
- DMF increased testosterone production and modulated key protein expressions (Nrf-2, HO-1, IL-10, β-Catenin, OCT-4, 3β-HSD, Bcl-2, NF-κB, Bax).
Conclusions:
- Dimethyl Fumarate (DMF) demonstrates a significant protective effect against testicular damage induced by Type 1 Diabetes Mellitus (T1DM) in Sprague-Dawley (SD) rats.
- DMF's protective mechanism involves reducing oxidative stress, apoptosis, and enhancing testosterone production through Nrf-2 activation.
